NF-κB partly mediated resveratrol (Res) inhibition on PKD inflammation. (A) Expression of p-p65, p65, p105, p50, TNF-α, MCP-1 and CFB in QNZ-treated OX161 cells. (B) OX161 cells were pretreated with QNZ for 2 h and followed by the treatment of resveratrol for 46 h. The expression of p-p65, p65, p105, p50, TNF-α, MCP-1 and CFB were evaluated by western blot. (C) MCP-1 or CFB of QNZ-and/or resveratroltreated OX161 cell supernatants were measured by ELISA. One representative of three independent experiments is shown.

Effect of NC1, NC1-CUR, NC2 and NC2-CUR on SH-SY5Y cell viability. The cells were treated for 24 h with different dilutions(1:1, 1:2 and 1:4) of empty nanocapsules (NC1 and NC2) and nanocapsules containing curcumin (NC1-CUR and NC2-CUR) followed by measurement of cell viability by MTT reduction assay (panel A) and cell toxicity by LDH release assay (panel B). Data after normalization to vehicle-treated cells (100%, MTT assay) or to total LDH release (TritonX100-treated cells, 100%) are presented as a mean±SEM from 3-8 independent experiments with five replicates. *p < 0.05, **p < 0.01 and ***p

The population of cmyb1kdrl1 cells in Tg(cmyb:GFP/kdrl:mCherry) embryos was decreased in JSH-23–treated embryos. White arrowheads mark cmyb1kdrl1 cells in the AGM region at 36 hpf. Right panel, Quantification of cmyb1kdrl1 cells.

G. To evaluate effects of IKBKE/TBK1 inhibition on NF-κB signaling in Ewing, TC32 cells were incubated with CYT387 for six hours prior to stimulation with TNF-α (30 ng/mL). IκBα degradation was measured by harvesting TC32 cells thirty minutes after stimulation with TNF-α. TNF-α stimulation resulted in degradation of IκBα, and this effect was attenuated with CYT387 treatment. Parthenolide, an inhibitor of IκBα phosphorylation was used as a positive control. Similar effects of CYT387 activity were seen in HEK-293T cells which also express IKBKΕ. Nuclear extracts were prepared from TC32 cells harvested following forty-five minutes of TNF-α stimulation. Treatment with CYT387 resulted in decreased nuclear localization of NF-κB family proteins RelA/p65 and c-Rel. There was a modest impairment of p50 nuclear localization as compared to parthenolide and DMSO controls and no change in p52 nuclear localization. RelB (not shown) is not expressed in TC32 cells

NF-κB partly mediated resveratrol (Res) inhibition on PKD inflammation. (A) Expression of p-p65, p65, p105, p50, TNF-α, MCP-1 and CFB in QNZ-treated OX161 cells. (B) OX161 cells were pretreated with QNZ for 2 h and followed by the treatment of resveratrol for 46 h. The expression of p-p65, p65, p105, p50, TNF-α, MCP-1 and CFB were evaluated by western blot. (C) MCP-1 or CFB of QNZ-and/or resveratroltreated OX161 cell supernatants were measured by ELISA. One representative of three independent experiments is shown.

Effect of NC1, NC1-CUR, NC2 and NC2-CUR on SH-SY5Y cell viability. The cells were treated for 24 h with different dilutions(1:1, 1:2 and 1:4) of empty nanocapsules (NC1 and NC2) and nanocapsules containing curcumin (NC1-CUR and NC2-CUR) followed by measurement of cell viability by MTT reduction assay (panel A) and cell toxicity by LDH release assay (panel B). Data after normalization to vehicle-treated cells (100%, MTT assay) or to total LDH release (TritonX100-treated cells, 100%) are presented as a mean±SEM from 3-8 independent experiments with five replicates. *p < 0.05, **p < 0.01 and ***p

The population of cmyb1kdrl1 cells in Tg(cmyb:GFP/kdrl:mCherry) embryos was decreased in JSH-23–treated embryos. White arrowheads mark cmyb1kdrl1 cells in the AGM region at 36 hpf. Right panel, Quantification of cmyb1kdrl1 cells.

G. To evaluate effects of IKBKE/TBK1 inhibition on NF-κB signaling in Ewing, TC32 cells were incubated with CYT387 for six hours prior to stimulation with TNF-α (30 ng/mL). IκBα degradation was measured by harvesting TC32 cells thirty minutes after stimulation with TNF-α. TNF-α stimulation resulted in degradation of IκBα, and this effect was attenuated with CYT387 treatment. Parthenolide, an inhibitor of IκBα phosphorylation was used as a positive control. Similar effects of CYT387 activity were seen in HEK-293T cells which also express IKBKΕ. Nuclear extracts were prepared from TC32 cells harvested following forty-five minutes of TNF-α stimulation. Treatment with CYT387 resulted in decreased nuclear localization of NF-κB family proteins RelA/p65 and c-Rel. There was a modest impairment of p50 nuclear localization as compared to parthenolide and DMSO controls and no change in p52 nuclear localization. RelB (not shown) is not expressed in TC32 cells